Erythropoietin, also known as EPO, has been in the headlines lately because of its biggest fan, Lance Armstrong, and his superhuman feats in athletic ability.

EPO is also known to improve glucose metabolism but researchers are unsure of how it works. The following studyinvestigates how EPO improves glucose tolerance.

Three important factors in this study are Akt, IR and IRS1. Akt plays a key role in glucose metabolism, IR are insulin receptors, and IRS1 is instrumental in transmitting signals from the insulin and insulin-like growth factor-1 (IGF-1) receptors to intracellular pathways like Akt. Working in harmony, the team makes a well-balanced glucose metabolism.

Subjects were fed a high-fat diet for 12 weeks and then treated with EPO for 2 weeks. Measurements were taken to ascertain their glucose metabolism. EPO treatment significantly enhanced the levels of Akt, but not IR and IRS1. EPO treatment considerably reduced the body weights and the levels of fasting blood glucose and insulin.

Gluconeogenesis is a way the body obtains glucose supplies by making it from protein rather than taking it directly from the blood sugar. Somehow EPO inhibits this process from happening and at the same time, suppresses the backlash of inflammation in the liver. EPO dulls the insulin receptors, insulin secretion, and dimishes the stored body fat. Akt must trigger fat metabolism.

Lance Armstrong is not a fat rat. He’s won Tour de France seven times. However his choice performance enhancing drug is shown to enhance glucose tolerance and inhibit inflammation in rats that were fed high-fat diets.

In the event researchers find a way to parlay these findings into a safe treatment for diabetes, there could be passengers of the D-train legally doping to break world records. Membership has its privileges.